Ultrasound for renal failure (lecture at Diagnostic). What is glomerulonephritis
Glomerulonephritis is an inflammatory disease of the kidneys. The inflammatory process spreads to the glomeruli and renal tubules. The disease is independent in nature, but is sometimes accompanied by infective endocarditis, lupus or hemorrhagic vasculitis. Diagnosis of glomerulonephritis is based on ultrasound of the kidneys and urine tests according to Zimnitsky.
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When the disease occurs, both kidneys are affected. It quickly turns into an acute form. If you seek medical help in a timely manner, it is treated within 2 months. Subacute nephron damage is acute early in the disease and worsens over time. Possible development renal failure. The chronic form is asymptomatic at the onset of the disease. Gradually developing pathological changes. They lead to replacement connective tissue nephrons.
Diagnostics
Diagnosis of glomerulonephritis disease involves laboratory confirmation using urine and blood tests. In case of rapid development or occurrence chronic stage A kidney tissue biopsy is required. An important factor is instrumental examinations for correct diagnosis and differential diagnosis. Timely diagnostic procedures have a beneficial effect on treatment.
Basic Research
The first visual examination of the patient is aimed at determining external symptoms. Next, the doctor determines the presence of recent infectious diseases and measures blood pressure.
The symptoms of glomerulonephritis have many similarities with acute pyelonephritis, so the doctor always refers the patient to diagnostic procedures.
The patient is examined in the clinic, after which he is admitted to the hospital. The attending physician determines bed rest for him and prescribes strict diet. When conducting medical examinations, doctors often, after patients undergo laboratory tests, discover that they have glomerulonephritis, which occurs without characteristic symptoms.
Urine tests
To formulate a correct diagnosis, laboratory tests are required. Examinations for glomerulonephritis include a dynamic study of the composition of urine. Such examinations give a correct picture of the changes and course of the inflammatory process. Appointed general analysis urine, according to Nechiporenko and according to the Kakovsky-Addis method.
Characteristic signs of the disease are:
- oliguria – decrease in urine volume;
- hematuria - an increase in blood cells in the urine;
- proteinuria – increased content of protein compounds in urine.
Glomerulonephritis always occurs with proteinuria, which is typical when filtration in the kidneys is impaired. Diagnosing hematuria is important. It occurs as a result of inflammation of the glomeruli and, along with proteinuria, most qualitatively reflects the course of the disease and the dynamics of recovery. These symptoms indicate the persistence of the inflammatory process. On the 3rd day, oliguria can be observed, which is subsequently replaced by polyuria. If this symptom persists for more than 6 days, the patient’s life may be in danger.
Other research methods
It is acceptable to hold a special instrumental diagnostics. Inspection with the help of technical devices greatly simplifies the placement, especially in young children. For a more detailed study of the course of the disease, its treatment and determination of the onset of consequences dangerous to the patient’s health, various technical tools are used: endoscopy, X-rays, computed tomography and ultrasound radiation.
Blood analysis
Using a blood test, you can determine the level of nitrogen in protein compounds. The composition begins to change if the amount of water increases. To exclude the diagnosis of acute pyelonephritis, a special immunological test is used to determine the true cause of the disease. It is two-level - the first helps to identify disorders in the body’s immune system, and the second helps to identify changes.
Differential diagnosis
Diagnosis of differential is based on study using the exclusion method. The presence of symptoms and laboratory tests allows you to compare data using logical analysis algorithms and separate diseases with similar characteristics. Glomerulonephritis is similar in its symptoms to many kidney diseases. This is the difficulty of determining by differential diagnosis. By exclusion, tuberculosis, pyelonephritis, kidney tumor and nephropathy must be excluded.
Ultrasound
The diagnosis of glomerulonephritis using ultrasound is quite easy to distinguish from other diseases by some specific signs: changes in the tubules and connective tissues, tissue thickening, diffuse transformations of the glomeruli, increased volume. A characteristic feature is also a cluster excess liquid in internal organs, which confirms the diagnosis.
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Glomerulonephritis in adults and children: causes of its occurrence, signs and symptoms, diagnosis, as well as effective methods of therapy
Glomerulonephritis is a bilateral inflammatory pathology of the kidneys. accompanied by damage to small renal vessels. With the development of this disease, there is a disruption in the main work of this organ: the formation of urine, cleansing the body of both toxic and unnecessary substances. This disease can affect a person of any age, however, in most cases, this pathology is observed in people under the age of forty. In representatives of the stronger sex, glomerulonephritis is observed much more often than in representatives of the weaker sex. In childhood, this disease is observed very often. In terms of its prevalence, it ranks second after infectious pathologies of the urinary system among all kidney diseases. The most common cause of the development of this pathological condition is considered to be the body’s reaction to various allergens and infections.
This disease is considered to be one of the most serious kidney diseases. Acute glomerulonephritis can almost always be completely cured. As for the chronic form of this pathology, it tends to cause the development of chronic renal failure. Patients with chronic renal failure require a kidney transplant and hemodialysis.
Glomerulonephritis – what is it?
Glomerulonephritis is the name given to acute or chronic inflammation of the kidney tissue, which is accompanied primarily by damage to the small vessels of the kidneys, as well as impaired kidney function to form urine. If we compare this disease with pyelonephritis, we can immediately draw attention to the fact that during its development, not one, but both kidneys are affected simultaneously.
Glomerulonephritis - what are the causes of its occurrence?
Among the most common reasons contributing to the development of this pathology are:
Infections. In most cases, the development of this pathology is a consequence of exposure of the human body to group beta hemolytic streptococcus A twelfth type. The same disease can make itself felt as a result of scarlet fever. tonsillitis. pharyngitis. as well as some other pathologies of an inflammatory and infectious nature. In the population of countries with hot climates, this disease occurs, as a rule, due to streptococcal lesions of the skin, namely phlyctena, as well as bullous streptococcal impetigo. Most often, when this pathology develops, doctors are able to identify the source of the infection.
Toxic components. The main toxic components that tend to cause the development of this disease include lead, alcoholic beverages, mercury, as well as organic solvents such as acetone, ethyl alcohol, gasoline, xylene, and so on.
Introduction of vaccinations. medications and serums also quite often provoke the occurrence of this disease.
Hypothermia in most cases it causes the development of “trench” nephritis. With hypothermia, there is a disturbance in the blood supply to the kidneys, as well as the development of an inflammatory process in this area.
Glomerulonephritis accompanies a huge number of systemic pathologies, namely infective endocarditis . systemic lupus erythematosus. hemorrhagic vasculitis and many others.
The main mechanism of development of glomerulonephritis in adults and children
A special role in the occurrence of this disease is played by immune reactions the human body to certain allergens or infections. Already two to three weeks after the infection affects the body, antibodies begin to be produced in the human blood, which tend to resist infection, while forming complexes of the so-called antigen-antibody. If the patient's blood shows a large number of infection antigens, then together with the same amount of antibodies they form heavy antigen-antibody complexes, which in turn move to the area of inflammation and initiate it.
This kind of inflammatory process tends not only to damage the kidneys, but also to disrupt their performance. As a result, glomerulonephritis occurs not so much due to infection, but as a result of the human body’s reaction to it. Allergic reactions, as well as inflammatory diseases such as chronic tonsillitis, can provoke the occurrence of this pathology. angina and others.
In childhood, this disease in most cases makes itself felt approximately two to three weeks after scarlet fever or sore throat. With this disease, in contrast to pyelonephritis. Both kidneys are affected, and always.
Glomerulonephritis in children and adults – what can it be? Forms of glomerulonephritis
The main forms of this disease include:
Signs and symptoms accompanying glomerulonephritis in adults and children
All signs and symptoms of this pathology are determined by its form.
Acute glomerulonephritis and its symptoms
Signs and symptoms of this pathology can be very diverse. They can be either invisible or pronounced.
The main symptoms and signs include:
As soon as certain signs of this pathology become apparent, a person should make an appointment with a nephrologist as soon as possible and undergo all the necessary examinations.
Parents whose children have been ill scarlet fever or sore throat. special attention should be paid to general condition baby's health. Signs of this pathology in children can become apparent only two to four weeks after a sore throat or scarlet fever.
Subacute glomerulonephritis and its symptoms
This form of glomerulonephritis is considered to be the most complex. In most cases, it is observed in adults. This disease is accompanied by serious changes in the urine ( red blood cells and protein are observed in the urine), constant increase blood pressure, as well as edema. The signs and symptoms of subacute glomerulonephritis are similar to those of the acute form of this pathology. The only one distinctive feature in this case, it is generally accepted to consider a lower, but longer temperature. Plus, this form of this disease tends to cause the development of certain complications much faster.
In this case, after a few weeks the patient experiences complete loss of kidney function. As a result, the patient undergoes dialysis and receives a kidney transplant.
Chronic glomerulonephritis and its symptoms
This form of glomerulonephritis tends to develop over a fairly long period of time. Sometimes this pathology is not accompanied by any symptoms at all, which is why it cannot be detected in a timely manner. In this case, the development of the disease is most often not interconnected with one or another acute inflammatory process. This pathology is accompanied by a very slow decrease in kidney function, as well as a gradual increase in blood pressure.
Prolonged lack of treatment for this pathology can cause chronic renal failure. In case of development of chronic renal failure, significant deterioration is observed general well-being patient. As a result, without a course of therapy, a person dies. In most cases, chronic renal failure contributes to the development uremia. Uremia is a pathology accompanied by the accumulation of large amounts of urea in the blood, as well as damage to various systems and organs of the human body. The brain is especially severely affected.
The signs and symptoms observed with uremia include:
Methods for diagnosing glomerulonephritis
The main methods for diagnosing this pathology include:
Glomerulonephritis during pregnancy
In most cases, during pregnancy, women experience an acute form of this disease. It occurs in pregnant women for the same reasons as in all other cases. The most common cause of the development of this pathology is considered to be infections of the ENT organs, as well as the throat, which could not be completely eliminated before the baby was conceived. It is not easy to identify the presence of this pathology in a pregnant woman, and all because this disease causes symptoms that can occur even in healthy expectant mothers. These include excessive fatigue, swelling, and painful sensations in the lumbar region, and so on. The main method for detecting this disease in a pregnant woman is still a general urine test, which reveals an excessive amount of red blood cells and protein.
Glomerulonephritis, as well as complications that arise against the background of this pathology, tend to greatly complicate the course of pregnancy. That is why there are cases when, in order to save the life of a mother suffering from this pathology, it is necessary to terminate the pregnancy. Let us note right away that this happens extremely rarely.
Therapy for this disease during pregnancy includes:
Treatment of this pathology during pregnancy should be carried out under the strict supervision of nephrologists and gynecologists.
Therapy of glomerulonephritis in adults and children
Treatment for this disease is carried out in the nephrology department of the hospital. In most cases, patients end up in this department in very serious condition.
Treatment of acute glomerulonephritis
Therapy for this form of this disease involves the use of both diuretics and antibiotics. In addition, patients are advised to follow a special diet. The course of therapy in this case takes about ten days. Considering the fact that this pathology most often occurs due to streptococcal throat infection, the patient may also be prescribed penicillin drugs such as Amoxicillin. Benzylpenicillin procaine. and Phenoxymethylpenicillin. The exact dosage will be indicated by a specialist. For children whose body weight does not exceed thirty kilograms, this medication is prescribed in the amount of two hundred and fifty milligrams every eight hours. If the child’s body weight is from thirty to fifty kilograms, then he is prescribed two hundred fifty to five hundred milligrams this drug every eight hours. For adolescents, as well as adults whose weight is less than eighty kilograms, five hundred milligrams are prescribed every eight hours. If edema develops, it is very important to use diuretics such as Ethacrynic acid. Hypothiazide. Furosemide. With the development of arterial hypertension, one cannot do without the help of angiotensin converting enzyme inhibitors, as well as diuretics. These pharmaceuticals include: Berlipril. so and Captopril. and Enalapril .
Diet for acute glomerulonephritis
In the fight against this pathology, it is very important to adhere to special diet. Patients are advised to reduce to a minimum the amount of fluid consumed, as well as salt and protein. A patient can eat no more than two grams of salt per day. Among food products that contain protein, you should give your preference to egg whites and cottage cheese. As for fats, you can eat no more than fifty grams of them per day. The normal daily amount of fluid in this case is considered to be six hundred to a thousand milliliters. Such patients are strictly prohibited from using meat soups. In most cases, a correct and timely course of therapy makes it possible not only to heal the patient, but also to completely restore the functioning of his kidneys.
Therapy of subacute and chronic glomerulonephritis
If we take into account information regarding the mechanism of development of glomerulonephritis, therapy for both subacute and chronic forms of this pathology involves getting rid of the three most important links in the occurrence of this disease. In this case, attention is paid to the immune response, immune inflammation and sclerotic processes in the kidneys.
Suppression of the immune response
Most often, to suppress the immune response, doctors prescribe to their patients immunosuppressants .
These include:
The effectiveness of therapy for the chronic form of this pathology is determined by the moment of treatment initiation. In general, the sooner therapy is started, the greater the patient’s chances of healing completely. Even if the patient manages to completely get rid of this disease, he will in any case have to regularly visit the doctor for a very long period of time. In order to prevent the development of this pathology, it is necessary to promptly treat infectious pathologies of the nasopharynx, as well as harden the body.
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Tests for glomerulonephritis
Timely diagnosis of glomerulonephritis and treatment are very important. They are able to prevent the severe course of this disease, which may lead to the development of chronic renal failure. The causes of glomerulonephritis often remain unclear. This is a collective definition of kidney diseases that are different in outcome, course and origin. At this time, only infectious signs have been well studied.
What is the disease?
Glomerulonephritis is an immunoinflammatory, immunoallergic group of diseases associated with damage to the vessels of the glomerular apparatus of both kidneys, changes in the structure of capillary membranes and impaired filtration. This leads to toxicity and excretion through urine necessary for the body protein components, blood cells. The disease occurs in people under 40 years of age and in children. The course of the disease is divided into the following types:
- spicy;
- subacute;
- chronic;
- focal nephritis.
- swelling;
- shortness of breath;
- flakes and particles of blood in urine;
- cyanosis of the lips;
- significant weight gain;
- slow heartbeat;
- small volume of urine.
- proteinuria - increased protein content;
- hematuria - the presence of blood particles in excess of the norm;
- oliguria - a sharp decrease in the volume of excreted fluid.
Causes
Sinusitis can trigger the occurrence of glomerulonephritis.
This immune-inflammatory disease is possible after diphtheria, bacterial endocarditis, malaria, typhoid fever, various types of pneumonia. It can develop due to repeated injections of serum vaccines, under the influence of medications, alcohol, drugs, injuries and hypothermia, especially in a humid environment. The occurrence of glomerulonephritis in children is a consequence of past streptococcal infections, such as scarlet fever, inflammation of the tonsils (tonsillitis), otitis media, sinusitis and dental granuloma. It progresses quickly and in most cases is completely cured.
External symptoms
External signs of chronic glomerulonephritis depend on the course of the disease. There are two options: classic (typical) and latent (atypical). In the atypical variant, swelling is poorly manifested and moderate disturbances in urination are slightly visible. The classic version is associated with infectious diseases; its symptoms are pronounced:
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Diagnostic procedures and tests for glomerulonephritis
Diagnosis of acute glomerulonephritis requires serious laboratory tests of blood and urine. With the rapid development of the disease and chronic form, a kidney biopsy may be needed to study the kidney tissue and immunological tests. An important factor in making a diagnosis are instrumental examinations and differential diagnosis. Timely diagnostic procedures facilitate the treatment of chronic glomerulonephritis.
First appointment
At the first appointment, the patient is examined for external signs of acute glomerulonephritis. Then the transferred ones are clarified 10-20 days before the examination infectious diseases, hypothermia, the presence of kidney disease, blood pressure is measured. Because the visible symptoms are similar to the signs of acute pyelonephritis; to establish the correct diagnosis, the doctor prescribes additional diagnostic procedures. The person is immediately sent to the hospital and is prescribed bed rest and diet.
Laboratory research
Laboratory tests help make an accurate diagnosis.
Laboratory diagnostics is an opportunity to make the correct diagnosis. Examination for glomerulonephritis includes a systematic study of the composition of urine and blood, which gives a correct idea of inflammatory processes in the body. For the study, a general urine test is prescribed, according to Nechiporenko and according to the Kakovsky-Addis method. Signs of acute glomerulonephritis:
Urine tests
Proteinuria is the main symptom of glomerulonephritis. This is due to a violation of filtration. Hematuria is an important symptom for diagnosis; it is a consequence of the destruction of glomerular capillaries. Along with proteinuria, it accurately shows the dynamics of the disease and the healing process. Enough for a long time these symptoms persist, signaling an unfinished inflammatory process. Oliguria is observed on days 1-3, then it is replaced by polyuria. The persistence of this symptom for more than 6 days is dangerous.
Blood tests
At the onset of the disease, a blood test shows a moderate increase in nitrogen-containing protein processing products. Additionally, its composition changes due to the high water content in the blood. An immunological two-level test is performed, which indicates the cause of the disease and excludes the diagnosis of acute pyelonephritis. The first level checks for gross violations in the immune system, the second is carried out to clarify the detected changes.
Instrumental diagnostics
This type of diagnosis is carried out using special medical equipment. Examination using technology simplifies the procedure for diagnosing glomerulonephritis in children because it is painless. X-rays are used to study the course of the disease, treatment, and identify dangerous changes in the kidney tissue. ultrasound scanning, computed tomography, various ways endoscopy.
Ultrasound diagnostics
Chronic glomerulonephritis on ultrasound can be distinguished from other nephrotic diseases by the following characteristics: sharp tissue thickening, increased volume with smooth and clear contours, diffuse changes in the glomeruli, connective tissues and tubules. These indicators differ from the signs of acute pyelonephritis, which simplifies the differential diagnosis. Ultrasound examination shows the accumulation of fluid in the organs, which also determines acute glomerulonephritis.
Kidney biopsy
Nephrobiopsy or kidney biopsy is a procedure in which a small piece of kidney tissue is pinched off for examination. This method accurately classifies immune complexes, which makes it possible to determine the type, form, cause, nature of changes and severity of the disease. The difficult definition of chronic glomerulonephritis makes a biopsy an indispensable examination.
Differential diagnosis
Differential diagnostics works by the method of exclusion. A doctor, having a mosaic of symptoms and laboratory tests, using a combination of logical and diagnostic algorithms, can distinguish between similar diseases. Acute and chronic glomerulonephritis is similar in symptoms to many diseases. This makes differential diagnosis more complicated. We will have to exclude acute pyelonephritis, nephropathy in diabetes, tuberculosis and tumor of the kidneys or urinary tract and many other nephrosis.
Chronic glomerulonephritis - description, causes, symptoms (signs), diagnosis, treatment.
Short description
Chronic glomerulonephritis(CGN, slowly progressive glomerular disease, chronic nephritic syndrome) is a group concept that includes diseases of the glomeruli of the kidney with a general immune mechanism of damage and a gradual deterioration of renal function with the development of renal failure.
Code by international classification diseases ICD-10:
- N03 Chronic nephritic syndrome
CLASSIFICATION
Clinical(Tareev E.M. Tareeva I.E. 1958, 1972). By form.. Latent form.. Hematuric form (see Berger's disease).. Hypertensive form.. Nephrotic form.. Mixed form. By phases.. Exacerbation ( active phase) - increasing changes in urine (proteinuria and/or hematuria), the appearance of acute nephritic or nephrotic syndrome, decreased renal function. Remission - improvement or normalization of extrarenal manifestations (edema, arterial hypertension), renal function and changes in urine.
Morphological(Serov V.V. et al. 1978, 1983) includes eight forms of CGN. Diffuse proliferative glomerulonephritis (see Acute glomerulonephritis). Glomerulonephritis with crescents (see Rapidly progressive glomerulonephritis). Mesangioproliferative glomerulonephritis. Membranous glomerulonephritis. Membrane - proliferative (mesangiocapillary) glomerulonephritis. Focal - segmental glomerulosclerosis. Fibroplastic glomerulonephritis.
Statistical data. Incidence is 13-50 cases per 10,000 population. Primary CGN occurs 2 times more often in men than in women, secondary - depending on the underlying disease. It can develop at any age, but most often in children 3-7 years old and adults 20-40 years old.
Causes
The same etiological factor can cause different morphological and clinical options nephropathies and, conversely, different reasons can cause the same morphological variant of damage.
Diffuse proliferative - see Acute glomerulonephritis.
Glomerulonephritis with crescents (see Rapidly progressive glomerulonephritis).
Mesangioproliferative glomerulonephritis - hemorrhagic vasculitis, chronic viral hepatitis B, Crohn's disease, Sjögren's syndrome, ankylosing spondylitis, adenocarcinomas.
Membranous glomerulonephritis - carcinomas of the lung, intestines, stomach, mammary glands and kidneys (paraneoplastic glomerulonephritis), non-Hodgken lymphoma, leukemia, SLE (see Lupus nephritis), viral hepatitis B, syphilis, filariasis, malaria, schistosomiasis, exposure to drugs (gold and mercury, as well as trimethadione and penicillamine).
Membrane - proliferative glomerulonephritis - idiopathic, as well as secondary to SLE, cryoglobulinemia, chronic viral (HCV) or bacterial infections, drugs, toxins.
CGN with minimal changes- idiopathic, as well as acute respiratory infections, vaccinations, NSAIDs, rifampicin or a - IFN, Fabry disease, diabetes, lymphoproliferative pathology (Hodgken lymphoma).
Focal segmental glomerulosclerosis - idiopathic, as well as sickle cell anemia, kidney transplant rejection, cyclosporine, surgical excision of part of the renal parenchyma, chronic vesicoureteral reflux, heroin use, congenital pathology (nephron dysgenesis, late stages of Fabry disease), HIV infection.
Immune mechanisms are involved in the development and maintenance of inflammation.. Immunocomplex.. Antibody (autoantigen).. Activation of complement, attraction of circulating monocytes, synthesis of cytokines, release of proteolytic enzymes and oxygen radicals, activation of the coagulation cascade, production of pro-inflammatory Pg.
In addition to immune and non-immune mechanisms, the progression of CGN involves.. Intraglomerular hypertension and hyperfiltration.. Proteinuria (nephrotoxic effects of proteinuria have been proven).. Hyperlipidemia.. Excessive formation of oxygen free radicals and accumulation of lipid peroxidation products.. Excessive calcium deposition.. Intercurrent recurrent infections urinary tract.
Pathomorphology depends on morphological form CGN. In any form, signs of sclerosis are revealed varying degrees in the glomeruli and interstitium - synechiae, sclerotic glomeruli, tubular atrophy. Proliferation and activation of mesangial cells play a key role in the processes of accumulation and changes in the structure of the extracellular matrix, which ends in sclerosis of the glomerulus. Pathomorphological changes are of exceptional importance for the diagnosis of glomerulonephritis, because Diagnosis almost always requires a biopsy of the kidney tissue.
Diffuse proliferative - diffuse increase glomerular cell numbers due to infiltration of neutrophils and monocytes and proliferation of glomerular endothelium and mesangial cells.
Glomerulonephritis with crescents (rapidly progressive) - see Glomerulonephritis, rapidly progressive.
Mesangioproliferative - proliferation of mesangial cells and matrix.
Membrane - proliferative - diffuse proliferation of mesangial cells and infiltration of glomeruli by macrophages; increase in mesangial matrix, thickening and duplication basement membrane.
CGN with minimal changes - light microscopy without pathology, with electron microscopy - disappearance of podocyte feet.
Focal segmental glomerulosclerosis is segmental collapse of capillaries in less than 50% of glomeruli with deposition of amorphous hyaline material.
Membranous - diffuse thickening of the glomerular basement membrane with the formation of subepithelial projections surrounding deposits immune complexes(jagged appearance of the basement membrane).
Fibroplastic glomerulonephritis is the outcome of most glomerulopathies and is characterized by the severity of fibrotic processes.
Symptoms (signs)
Clinical manifestations. Symptoms appear 3-7 days after exposure to the provoking factor (latent period), and they can also be detected accidentally during a medical examination. Recurrent episodes of hematuria. Edema, urinary syndrome, arterial hypertension in various forms - nephrotic or acute nephritic syndrome (nephrotic form, mixed form - up to 10%, hypertensive form - 20-30%). A combination of manifestations of acute nephritic and nephrotic syndromes is possible. Complaints of headache, dark urine, swelling and decreased urine output. Objectively - pastosity or edema, increased blood pressure, expansion of the borders of the heart to the left. Body temperature is normal or subfebrile.
Clinical manifestations in various clinical forms
Latent CGN (50-60%) .. No edema or arterial hypertension.. In urine proteinuria no more than 1-3 g/day, microhematuria, leukocyturia, casts (hyaline and erythrocyte)... Can transform into nephrotic or hypertensive forms.. The development of chronic renal failure occurs over 10-20 years.
Hypertensive chronic hepatitis.. Clinical manifestations of arterial hypertension syndrome.. There is slight proteinuria in the urine, sometimes microhematuria, cylindruria.. Chronic renal failure develops over 15-25 years.
Hematuric CGN.. In the urine - recurrent or persistent hematuria and minimal proteinuria (less than 1 g/day).. There are no extrarenal symptoms.. CRF develops in 20-40% over 5-25 years.
Nephrotic form - clinical - laboratory manifestations nephrotic syndrome.
Mixed form.. Combination of nephrotic syndrome, arterial hypertension and/or hematuria.. It is usually noted in secondary CGN, systemic diseases (SLE, systemic vasculitis).. CRF develops within 2-3 years.
Clinical picture depending on the morphological form
Mesangioproliferative CGN.. Isolated urinary syndrome.. Acute nephritic or nephrotic syndrome.. Macro - or microhematuria - Berger's disease.. CRF develops slowly.
Membranous CGN manifests itself as nephrotic syndrome (80%).
Membrane - proliferative CGN.. Begins with acute nephritic syndrome, in 50% of patients - nephrotic syndrome.. Isolated urinary syndrome with hematuria.. Arterial hypertension, hypocomplementemia, anemia, cryoglobulinemia are characteristic.. The course is progressive, sometimes rapidly progressive.
Glomerulonephritis with minimal changes.. Nephrotic syndrome, in 20-30% of cases with microhematuria.. Arterial hypertension and renal failure occur rarely.
Focal - segmental glomerulosclerosis.. Nephrotic syndrome.. Erythrocyturia, leukocyturia in the urine.. Arterial hypertension.. The natural development of chronic renal failure.
Fibroplastic glomerulonephritis.. Nephrotic syndrome (up to 50%).. Chronic renal failure.. Arterial hypertension.
Diagnostics
Laboratory data
In the blood - moderate increase in ESR(with secondary CGN, a significant increase may be detected, which depends on primary disease), an increase in the level of CEC, antistreptolysin O, a decrease in the content of complement in the blood (immune complex CGN), with Berger's disease an increase in the content of IgA is detected.
The concentrations of total protein and albumin are reduced (significantly in nephrotic syndrome), the concentrations of a 2 - and b - globulins are increased, hypogammaglobulinemia is observed in nephrotic syndrome. In secondary CGN caused by systemic connective tissue diseases (lupus nephritis), g-globulins may be increased. Hyper- and dyslipidemia (nephrotic form).
Decreased GFR, increased levels of urea and creatinine, anemia, metabolic acidosis, hyperphosphatemia, etc. (ARI due to chronic renal failure or chronic renal failure).
In the urine there is erythrocyturia, proteinuria (massive in nephrotic syndrome), leukocyturia, casts are granular, waxy (in nephrotic syndrome).
Instrumental data. With ultrasound or survey urography, the size of the kidneys is normal or reduced (with chronic renal failure), the contours are smooth, and the echogenicity is diffusely increased. X-ray of organs chest- expansion of the borders of the heart to the left (with arterial hypertension). ECG - signs of left ventricular hypertrophy. Kidney biopsy (light, electron microscopy, immunofluorescence study) allows you to clarify the morphological form and activity of CGN, and exclude kidney diseases with similar symptoms.
Diagnostics. With a decrease in diuresis, the appearance of dark urine, swelling or pastiness of the face, increased blood pressure (may be normal), a set of studies is carried out: measurement of blood pressure, total blood flow, total blood volume, determination of daily proteinuria, total protein concentration and evaluate the proteinogram, lipid content in the blood. In-depth physical and clinical – laboratory examination aimed at identifying possible reason CGN - general or systemic disease. Ultrasound (x-ray) of the kidneys allows you to clarify the size and density of the kidneys. Assessment of kidney function - Reberg-Tareev test, determination of the concentration of urea and/or creatinine in the blood. The diagnosis is confirmed by a kidney biopsy.
Differential diagnosis: with chronic pyelonephritis, acute glomerulonephritis, nephropathy of pregnancy, chronic tubulo-interstitial nephritis, alcoholic kidney damage, amyloidosis and diabetic nephropathy, as well as kidney damage in diffuse connective tissue diseases (primarily SLE) and systemic vasculitis.
Treatment
General tactics. Hospitalization in the hospital for exacerbation of CGN, newly diagnosed CGN, newly diagnosed chronic renal failure. A diet with limited salt (for edema, arterial hypertension), protein (for chronic renal failure, exacerbation of chronic hypertension). Impact on the etiological factor (infection, tumors, drugs). Immunosuppressive therapy - GCs and cytostatics - for exacerbation of CGN (indicated also for azotemia, if it is caused by the activity of CGN). Antihypertensive drugs. Antiplatelet agents, anticoagulants. Antihyperlipidemic drugs. Diuretics.
Immunosuppressive therapy
GCs are indicated for mesangioproliferative CGN and CGN with minimal changes in the glomeruli. With membranous CGN, the effect is unclear. For membrano-proliferative CGN and focal-segmental glomerulosclerosis, GCs are ineffective. Prednisolone is prescribed 1 mg/kg/day orally for 6-8 weeks, followed by rapid decline up to 30 mg/day (5 mg/week), and then slowly (2.5-1.25 mg/week) until complete withdrawal.. Pulse - prednisolone therapy is carried out with high CGN activity in the first days of treatment - 1000 mg IV drip 1 time per day for 3 days in a row. After CGN activity decreases, monthly pulse therapy is possible until remission is achieved.
Cytostatics (cyclophosphamide 2-3 mg/kg/day orally or intramuscularly or intravenously, chlorambucil 0.1-0.2 mg/kg/day orally, as alternative drugs: cyclosporine - 2.5- 3.5 mg/kg/day orally, azathioprine 1.5-3 mg/kg/day orally) are indicated for active forms CGN with high risk progression of renal failure, as well as in the presence of contraindications for the use of GCs, ineffectiveness or complications when using the latter (in the latter case, combined use is preferred, allowing a reduction in the dose of GCs). Pulse - cyclophosphamide therapy is indicated for high CGN activity, either in combination with pulse - therapy with prednisolone (or against the background of daily oral prednisolone), or alone without additional prescription of prednisolone; in the latter case, the dose of cyclophosphamide should be 15 mg/kg (or 0.6-0.75 g/m2 body surface area) IV monthly.
The simultaneous use of GC and cytostatics is considered more effective than GC monotherapy. It is generally accepted to prescribe immunosuppressive drugs in combination with antiplatelet agents, anticoagulants - the so-called multicomponent regimens: ... 3 - component regimen (without cytostatics) ... Prednisolone 1-1.5 mg/kg/day orally for 4-6 weeks, then 1 mg/kg/day after day, then reduced by 1.25-2.5 mg/week until discontinuation... Heparin 5000 units 4 times a day for 1-2 months with a transition to phenindione or acetylsalicylic acid at a dose of 0.25-0.125 g/ day, or sulodexide at a dose of 250 IU 2 times/day orally... Dipyridamole 400 mg/day orally or intravenously.. 4-component Kinkaid-Smith scheme... Prednisolone 25-30 mg/day orally for 1-2 months, then dose reduction by 1.25-2.5 mg/week until discontinuation... Cyclophosphamide 200 mg IV daily or double dose every other day for 1-2 months, then half dose until remission decreases (cyclophosphamide can be replaced with chlorambucil or azathioprine) ... Heparin 5000 units 4 times a day for 1-2 months with a transition to phenindione or acetylsalicylic acid, or sulodexide ... Dipyridamole 400 mg / day orally or intravenously .. Ponticelli scheme: start of therapy with prednisolone - 3 days in a row at 1000 mg/day, the next 27 days prednisolone 30 mg/day orally, 2nd month - chlorambucil 0.2 mg/kg.. Steinberg scheme... Pulse - cyclophosphamide therapy: 1000 mg IV monthly for a year... In the next 2 years - once every 3 months... In the next 2 years - once every 6 months.
Symptomatic therapy
Antihypertensive therapy... ACE inhibitors have antiproteinuric and nephroprotective effects, because by reducing intraglomerular hyperfiltration and hypertension, they slow down the rate of progression of chronic renal failure: captopril 50-100 mg/day, enalapril 10-20 mg/day, ramipril 2.5-10 mg/day. Non-hydropyridine calcium channel blockers: verapamil in a dose 120-320 mg/day, diltiazem at a dose of 160-360 mg/day, isradipine, etc.
Diuretics - hydrochlorothiazide, furosemide, spironolactone.
Antioxidant therapy (vitamin E), but there is no convincing evidence of its effectiveness.
Lipid-lowering drugs (nephrotic syndrome): simvastatin, lovastatin, fluvastatin, atorvastatin at a dose of 10-60 mg/day for 4-6 weeks, followed by a dose reduction.
Anticoagulants (in combination with GC and cytostatics, see above).. Heparin 5000 IU 4 times a day subcutaneously (under the control of the international normalized ratio [INR]) for at least 1-2 months; before discontinuation, reduce the dose 2-3 days before discontinuation. Low molecular weight heparins: nadroparin calcium in a dose of 0.3-0.6 ml 1-2 r/day subcutaneously, sulodexide intramuscularly 600 IU 1 r/day for 20 days, then orally 250 IU 2 r/day.
Antiplatelet agents (in combination with GCs, cytostatics, anticoagulants; see above) .. Dipyridamole 400-600 mg/day .. Pentoxifylline 0.2-0.3 g/day .. Ticlopidine 0.25 g 2 r/ day.. Acetylsalicylic acid 0.25-0.5 g/day.
The following therapeutic measures are also used in the treatment of CGN (the effect of which has not been proven in controlled studies).
NSAIDs (an alternative to prednisolone for low clinical activity CGN): indomethacin 150 mg/day for 4-6 weeks, then 50 mg/day for 3-4 months (contraindicated in arterial hypertension and renal failure).
Aminoquinoline derivatives (chloroquine, hydroxychloroquine) are prescribed in the absence of indications for active therapy for sclerosing forms, 0.25-0.2 g orally 2 times a day for 2 weeks, then 1 time a day.
Plasmapheresis in combination with pulse therapy with prednisolone and/or cyclophosphamide is indicated for highly active CGN and there is no effect from treatment with these drugs.
Treatment of individual morphological forms
Mesangioproliferative CGN.. With slowly progressing forms, incl. with IgA nephritis, there is no need for immunosuppressive therapy.. With a high risk of progression - GC and/or cytostatics.. 3- and 4-component regimens.. The effect of immunosuppressive therapy on long-term prognosis remains unclear.
Membranous CGN.. Combined use of GC and cytostatics.. Pulse - therapy with cyclophosphamide 1000 mg IV monthly.. In patients without nephrotic syndrome and normal function kidneys - ACE inhibitors.
Membrane-proliferative (mesangiocapillary) CGN.. Treatment of the underlying disease.. ACE inhibitors.. In the presence of nephrotic syndrome and decreased renal function, therapy with GC and cyclophosphamide with the addition of antiplatelet agents and anticoagulants is justified.
CGN with minimal changes.. Prednisolone 1-1.5 mg/kg for 4 weeks, then 1 mg/kg every other day for another 4 weeks.. Cyclophosphamide or chlorambucil if prednisolone is ineffective or cannot be discontinued due to relapses. For continuing relapses of nephrotic syndrome - cyclosporine 3-5 mg/kg/day (children 6 mg/m2) for 6-12 months after achieving remission.
Focal segmental glomerulosclerosis. Immunosuppressive therapy is not effective enough. GCs are prescribed for a long time - up to 16-24 weeks. Patients with nephrotic syndrome are prescribed prednisolone 1-1.2 mg/kg daily for 3-4 months, then every other day for another 2 months , then the dose is reduced until discontinuation. Cytostatics (cyclophosphamide, cyclosporine) in combination with GC.
Fibroplastic CGN.. With a focal process, treatment is carried out according to the morphological form that led to its development.. Diffuse form- contraindication to active immunosuppressive therapy.
Treatment by clinical forms carried out if it is impossible to perform a kidney biopsy.
Latent form. Active immunosuppressive therapy is not indicated. For proteinuria >1.5 g/day, ACE inhibitors are prescribed.
Hematuric form.. Inconsistent effect of prednisolone and cytostatics.. Patients with isolated hematuria and/or slight proteinuria - ACE inhibitors and dipyridamole.
Hypertensive form.. ACE inhibitors; target blood pressure level is 120-125/80 mm Hg. For exacerbations, cytostatics are used as part of a 3-component regimen. GC (prednisolone 0.5 mg/kg/day) can be prescribed as monotherapy or as part of combined regimens.
Nephrotic form is an indication for the use of a 3- or 4-component regimen.
Mixed form - 3 - or 4 - component treatment regimen.
Surgery. Kidney transplantation is complicated in 50% by graft relapse, and in 10% by graft rejection.
Features of the course in children. More often than in adults, post-streptococcal nephritis results in recovery. Nephrotic syndrome is up to 80% caused by CGN with minimal changes.
Features of the course in pregnant women. The effect of pregnancy on the kidneys: function decreases, the frequency of secondary gestosis increases. The effect of CGN on pregnancy - three degrees of risk (Shekhtman M.M. et al. 1989): .. I degree (minimal) - pregnancy can be resolved ( latent form) .. II degree (severe) - high risk (nephrotic form) .. III degree (maximum) - pregnancy is contraindicated (hypertensive and mixed forms, active CGN, chronic renal failure).
Complications. Renal failure, left ventricular failure, acute impairment cerebral circulation, intercurrent infections, thrombosis.
Course and prognosis. The frequency of progression to chronic renal failure depends on the morphological form of chronic renal failure. Diffuse proliferative - 1-2%. Mesangioproliferative - 40%. Rapidly progressive - 90%. Membranous - 40%. Focal and segmental glomerulosclerosis - 50-80%. Membranous - proliferative - 50%. IgA - nephropathy - 30-50%.
Reduction. CGN - chronic glomerulonephritis.
ICD-10. N03 Chronic nephritic syndrome
Three will be allowed classic symptoms: swelling, reddish urine and increased blood pressure, which may be accompanied by a headache or not bother the patient, determined only by measurement. The first appearance of these symptoms in young people is likely to lead to a diagnosis of acute glomerulonephritis. In old age, these changes in most cases will be attributed to primary chronic glomerulonephritis. Chronic glomerulonephritis is also diagnosed when acute glomerulonephritis exists within 12 months from the onset of the disease.
The diagnosis of rapidly progressive glomerulonephritis is usually made if, just a month and a half after the onset of the acute process, the density of urine decreases, nephrotic syndrome develops and blood pressure rises. This is accompanied by an increase in urea and creatinine in the blood.
Urine and blood tests and, if necessary, a kidney biopsy help confirm the diagnosis of glomerulonephritis. A general urine test reveals protein, a large number of red blood cells, and casts (casts of the renal tubules). A biochemical blood test for glomerulonephritis shows a decrease in total protein and an increase in its individual types.
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Kidney failure and other kidney problems are often detected through a standard urine test. A blood test may also be added to laboratory diagnostics. More complex instrumental diagnostic methods are used only to track the dynamics of changes in the structure of the kidneys. So, for example, glomerulonephritis on ultrasound, depending on the form of the pathology, may not give visible changes at all. Below you can find out how the pathology is formed and what is visible during ultrasound examination.
Glomerulonephritis: general picture of the disease and causes of its occurrence
Glomerulonephritis is a disorder of the glomerular filtration system in the kidneys. In this case, as a rule, both kidneys are affected at once. As a result of decreased glomerular performance, urine volume and quality decrease. That is, kidney failure develops.
Most often, the onset of the disease is caused by infectious diseases such as tonsillitis, scarlet fever, tonsillitis or purulent skin infection. In all these cases, the causative agent is streptococcal bacteria. The process of onset of glomerulonephritis in this case looks like this:
- The patient suffers from the above infections. After 10-14 days, visible complete recovery occurs.
- However, during the period of illness, the human body begins an internal struggle, which is expressed in an allergic reaction. As a result, antibodies are produced, which subsequently bind pathogenic microbial cells and carry them throughout the body along with the bloodstream.
- Next, the associated bacterial cells settle in glomerular apparatus kidneys, which are responsible for filtering blood. Thus, glomerulonephritis begins.
In addition, the causes of the onset of the disease can be:
- Banal and prolonged hypothermia in water;
- Past illnesses such as malaria or tuberculosis;
- Also, vaccination can be a provocateur of glomerulonephritis (if the body is weakened);
- An allergic reaction to certain groups of medications or toxins that have entered the body.
Forms of glomerulonephritis and their symptoms
Nephrologists divide the course of the disease into two forms - chronic and acute. In the first case, the patient may have virtually nothing to worry about. Only occasionally weakness and headache, as well as loss of appetite and fatigue will accompany the patient. But most often such symptoms are attributed to fatigue, vitamin deficiency and stress. The disease can be detected at this stage only through a general urine test.
Important: this is why it is necessary to regularly submit urine for general analysis in order to diagnose possible pathological changes in time.
If glomerulonephritis manifests itself in an acute form, then all the symptoms will already be evident. So, the general picture during exacerbation of renal failure will be as follows:
- Long-term nagging pain in the lumbar region.
- Reducing daily urine volume.
- Morning swelling that goes away by lunchtime.
- Discoloration of urine in a reddish tint. Moreover, urine can have a barely visible red color or have the appearance of meat juice.
- Possible nausea, vomiting, loss of appetite.
- Headache and increased body temperature up to 37.5 degrees also occur.
Important: if such symptoms appear, you must immediately go to the hospital to receive further treatment. Since acute glomerulonephritis has a negative effect on the cardiovascular system and brain.
Diagnosis of glomerulonephritis: blood and urine tests, ultrasound
In order to select the most effective treatment tactics, it is necessary to identify the nature of the disease (infectious/non-infectious) and establish the severity of its course (the extent to which the kidneys cannot cope with their function). The main laboratory tests for diagnosing glomerulonephritis are:
- General urine analysis. Here, specialists will identify the level of protein, which will indicate an inflammatory process in the urinary system. Also, during the analysis, the laboratory technician will determine the concentration of red blood cells in the patient’s urine. Their presence indicates that there is blood loss along with urine. Moreover, red blood cells can be either seen with the naked eye in the urine (macrohematuria) or seen only under a microscope (microhematuria). Determining the concentration of protein and red blood cells in the urine allows the attending physician to adjust the patient’s diet with glomerulonephritis. The diet will be aimed at reducing the amount of salt and protein, as well as correcting the drinking regime.
Important: within acute period illness, the patient must be on bed rest. This will relieve vasospasm and reduce blood pressure. As a result, the stress on the kidneys will be minimal, and the volume of urine will increase. This in turn neutralizes swelling.
- A general blood test during inflammatory processes will show an increased ESR (erythrocyte sedimentation rate).
- In addition, a biochemical blood test will be performed to diagnose the nature of the disease. And if it is determined that streptococcus is the causative agent of the pathology, then antibacterial therapy is used to treat the patient.
Ultrasound diagnosis of glomerulonephritis
Carrying out ultrasound examination, as a rule, is not particularly informative method diagnostics In this case, it is only possible to identify structural changes in the kidneys and their location. It is worth knowing that if glomerulonephritis is in a chronic form, then the specialist will not see any special changes on ultrasound. The structure of the kidneys and their shape will remain unchanged.
If glomerulonephritis is in an acute form, then the following changes can be noted on an ultrasound of the kidneys:
- Thickening of the parenchyma of both kidneys;
- Change in the contours of the kidneys to unclear;
- It is also possible to identify increased echogenicity, and against its background the presence of hypoechoic pyramids may be noted;
- Also, if ultrasound angiography is performed, the vascular pattern will be combined;
- If Doppler sonography is performed, then a reduced peripheral resistance index will be noted in the arcuate arteries. At the same time, in the segmental and interlobar arteries the resistance index values will be normal.
Important: the nephrologist uses all the data obtained to prescribe the most effective treatment for glomerulonephritis.
To completely recover from the disease, you must strictly adhere to all the recommendations of your doctor. Since often it is diet therapy and bed rest for 2-5 weeks that are the key to successful treatment. Drug therapy in this case, it relieves only the symptoms of the disease (normalizes blood pressure, reduces swelling, increases the volume of urine).
After successful treatment, active sports, severe physical work, hypothermia and overheating, swimming in ponds and working with chemicals. If possible, sanatorium-resort treatment is indicated.
Kidney ultrasound is a common procedure for diagnosing diseases of the urinary system. Sometimes Ultrasound carried out for preventive purposes early diagnosis possible diseases. In order to be able to distinguish kidney diseases from ultrasound images, it is necessary, first of all, to know the anatomy and normal ultrasound images of the kidneys. Kidney ultrasound has its own characteristics for different age periods Therefore, ultrasound images are evaluated differently for children and adults. Anatomy of the urinary system and kidneys
Normal and topographic anatomy form the basis of any study. To compare kidney ultrasound data and make a conclusion, you need to know the anatomical data, which is the norm. However, it is worth considering that the kidneys are an organ whose structure exhibits greatest number anatomical options.In case of renal circulatory disorders, ultrasound reveals following signs acute renal failure:
- the buds acquire a spherical shape;
- the boundary between the cortex and medulla is sharply emphasized;
- the kidney parenchyma is thickened;
- the echogenicity of the cortex is increased;
- Doppler examination reveals a decrease in blood flow velocity.
Kidney injury on ultrasound. Concussion ( injury), renal hematoma on ultrasound
Kidney injury occurs as a result of the application of external force to the lower back or abdomen due to strong blow or squeezing. Kidney disease makes them even more susceptible to mechanical damage. Most often, kidney injuries are closed, which is why the patient may not be aware of internal bleeding when the kidneys rupture.There are two types of kidney injuries:
- Bruise ( contusion). With a bruise, there are no ruptures of the capsule, parenchyma or renal pelvis. Such damage usually passes without consequences.
- Gap. When a kidney ruptures, the integrity of its tissues is compromised. Ruptures of the renal parenchyma lead to the formation of hematomas inside the capsule. In this case, blood can enter the urinary system and be excreted along with urine. In another case, when the capsule ruptures, blood along with primary urine flows into the retroperitoneal space. This is how the perinephric ( perirenal) hematoma.
The best diagnostic capabilities for injuries and hematomas are offered by computed tomography and magnetic resonance imaging. Treatment of hematomas with a volume of up to 300 ml is carried out conservatively. Sometimes percutaneous puncture of hematomas can be performed under ultrasound guidance. Only in 10% of cases with heavy internal bleeding, surgical intervention is performed.
Chronic renal failure ( chronic renal failure) on ultrasound
Chronic renal failure is a pathological decrease in kidney function as a result of the death of nephrons ( functional renal units). Chronic kidney failure is the outcome of most chronic kidney diseases. Because chronic diseases are asymptomatic, the patient considers himself healthy until the onset of uremia. In this condition, severe intoxication of the body occurs with those substances that are usually excreted in the urine ( creatinine, excess salts, urea).The causes of chronic renal failure are the following diseases:
- chronic pyelonephritis;
- chronic glomerulonephritis;
- urolithiasis disease;
- arterial hypertension ;
- diabetes;
- polycystic kidney disease and other diseases.
The following degrees of severity of chronic renal failure are distinguished depending on the glomerular filtration rate ( SCF):
- Easy. GFR ranges from 30 to 50 ml/min. The patient notices an increase in nighttime urine output, but nothing else bothers him.
- Average. GFR ranges from 10 to 30 ml/min. Daily urination increases and constant thirst appears.
- Heavy. GFR less than 10 ml/min. Patients complain about constant fatigue, weakness, dizziness. Nausea and vomiting may occur.
Signs of a wrinkled kidney ( nephrosclerosis) on ultrasound. Retraction of the renal parenchyma
The term "shrinked bud" ( nephrosclerosis) describes a condition in which kidney tissue is replaced by connective tissue. Many diseases cause destruction of the kidney parenchyma, and the body is not always able to replace dead cells identical. The human body does not tolerate emptiness, therefore, with massive cell death, regeneration occurs and they are replenished with connective tissue cells.Connective tissue cells produce fibers that, when attracted to each other, cause a decrease in the size of the organ. In this case, the organ shrinks and ceases to function fully.
At acute inflammation the kidneys increase in size, and hypoechoic swelling of the tissue around the organ forms. Chronic infection gradually leads to a decrease in kidney size. Accumulations of pus appear as hypoechoic areas. When there is inflammation in the kidney, blood flow may change. This is clearly visible on duplex ultrasound using Doppler mapping.
In addition to ultrasound, contrast contrast is used to visualize inflammatory processes in the kidneys. X-ray examination, computed and magnetic resonance imaging ( CT and MRI). If some areas of the kidneys are inaccessible for examination on x-rays, then tomography allows you to obtain a detailed image of the kidneys. However, there is not always time and appropriate conditions to perform CT and MRI.
Acute pyelonephritis on kidney ultrasound
Pyelonephritis is an infectious and inflammatory disease of the kidneys. In pyelonephritis, the renal parenchyma and collecting tubule system are affected. With this disease, the infection enters the kidney upward path through the ureters. Often acute pyelonephritis becomes a complication of cystitis - inflammation of the bladder. Pyelonephritis is caused mainly by opportunistic microflora ( coli) and staphylococci. Depending on its course, pyelonephritis can be acute or chronic.Symptoms of acute pyelonephritis are:
- fever, fever, chills;
- pain in the lumbar region;
- urinary disturbance ( decreased amount of urine).
Signs of acute pyelonephritis on kidney ultrasound are:
- an increase in the size of the kidneys more than 12 cm in length;
- decreased kidney mobility ( less than 1 cm);
- deformation of the medulla with the formation of accumulations of serous fluid or pus.
Kidney carbuncle on ultrasound. Kidney abscess
Kidney carbuncle and abscess are severe manifestations of acute purulent pyelonephritis. They represent a limited infectious process in the renal parenchyma. When an abscess forms, microorganisms enter the kidney tissue through the blood or ascending the urinary tract. An abscess is a cavity surrounded by a capsule, inside which pus accumulates. On ultrasound, it appears as a hypoechoic area in the renal parenchyma with a bright hyperechoic rim. Sometimes with an abscess there is an expansion of the pyelocaliceal system.A kidney carbuncle is more severe than an abscess. Carbuncle is also caused by the proliferation of microorganisms in the kidney tissue. However, in the mechanism of carbuncle development, the vascular component plays the main role. When microorganisms enter a vessel, they block its lumen and stop blood supply. In this case, the death of kidney cells occurs due to lack of oxygen. After thrombosis and heart attack ( vascular necrosis) the renal wall is followed by its purulent melting.
With a kidney carbuncle on ultrasound, the organ is enlarged and its structure is locally deformed. The carbuncle looks like a volumetric formation of high echogenicity with fuzzy outlines in the kidney parenchyma. In the center of the carbuncle there are hypoechoic areas corresponding to the accumulation of pus. In this case, there are usually no changes in the pyelocaliceal structure. Carbuncle and kidney abscess are treated surgically with the mandatory use of antibiotics.
Chronic pyelonephritis on kidney ultrasound
Chronic pyelonephritis differs from acute pyelonephritis in its long course and tendency to exacerbations. This disease is characterized by the persistence of foci of infection in the kidney tissue. It occurs due to a violation of the outflow of urine. Hereditary factors and acquired conditions are to blame for this ( for example, urolithiasis). With each exacerbation, chronic pyelonephritis affects more and more areas of the parenchyma, which is why the entire kidney gradually becomes non-functional.Chronic pyelonephritis has several phases changing each other in its course:
- Active phase. This phase proceeds similarly to acute pyelonephritis and is characterized by severe pain, malaise, and difficult urination.
- Latent phase. The patient is bothered by rare pain in the lower back, while bacteria are always present in the urine.
- Remission phase. It is a condition in which the disease does not manifest itself in any way, however, with a decrease in immunity, it can suddenly worsen.
Signs chronic pyelonephritis on ultrasound of the kidneys are:
- Expansion and deformation of the pyelocaliceal system. It becomes rounded, and the cups merge with the pelvis.
- Reduction in the thickness of the kidney parenchyma. The ratio of the kidney parenchyma to the pyelocaliceal system becomes less than 1.7.
- Reduction in kidney size uneven outline edges of the bud. This deformation indicates long term process and wrinkling of the kidney.
Glomerulonephritis on kidney ultrasound
Glomerulonephritis is an autoimmune lesion of the vascular glomeruli of the kidneys located in the renal cortex. The glomeruli are part of the nephron - functional unit kidney It is in the vascular glomeruli that blood filtration and the initial stage of urine formation occur. Glomerulonephritis is the main disease leading to chronic renal failure. When 65% of nephrons die, signs of renal failure appear.Symptoms of glomerulonephritis are:
- increased blood pressure;
- swelling;
- red coloration of urine ( presence of red blood cells);
- lower back pain.
IN initial stage Glomerulonephritis on ultrasound shows the following signs:
- increase in kidney volume by 10 - 20%;
- a slight increase in the echogenicity of the kidneys;
- increased blood flow velocity in the renal arteries;
- clear visualization of blood flow in the parenchyma;
- symmetrical changes in both kidneys.
- a significant decrease in the size of the kidneys, up to 6 – 7 cm in length;
- hyperechogenicity of kidney tissue;
- inability to distinguish between the renal cortex and medulla;
- decrease in blood flow velocity in the renal artery;
- depletion of the bloodstream inside the kidney.
Renal tuberculosis on ultrasound
Tuberculosis is a specific disease caused by mycobacterium. Kidney tuberculosis is one of the most common secondary manifestations of this disease. The primary focus of tuberculosis is the lungs, then Mycobacterium tuberculosis enters the kidneys through the bloodstream. Mycobacteria multiply in the glomeruli of the renal medulla.With tuberculosis in the kidneys, the following processes are observed:
- Infiltration. This process means the accumulation of mycobacteria in the cortex and medulla with the formation of ulcers.
- Tissue destruction. The development of tuberculosis leads to the formation of zones of necrosis, which look like rounded cavities.
- Sclerosis ( connective tissue replacement). The vessels and functional cells of the kidneys are replaced by connective tissue. This defensive reaction leads to impaired renal function and renal failure.
- Calcification ( calcification). Sometimes foci of mycobacteria multiplication turn into stone. This protective reaction of the body is effective, but does not lead to a complete cure. Mycobacteria can regain activity again when immunity decreases.
Anomalies of the structure and position of the kidneys on ultrasound. Kidney diseases accompanied by the formation of cysts
Kidney anomalies are abnormalities caused by abnormal embryonic development. For one reason or another, anomalies genitourinary system are the most common. It is believed that about 10% of the population has various kidney abnormalities. Kidney abnormalities are classified as follows:
- Abnormalities of the renal vessels. They consist of changing the trajectory, the number of renal arteries and veins.
- Abnormalities in the number of kidneys. There have been cases where a person had 1 or 3 kidneys. Separately, the anomaly of kidney duplication is considered, in which one of the kidneys is divided into two practically autonomous parts.
- Abnormalities in kidney size. The kidney may be reduced in size, but there are no cases of congenital enlarged kidneys.
- Abnormalities of the kidneys. The kidney may be located in the pelvis, near the iliac crest. There are also cases when both kidneys are located on the same side.
- Abnormalities of the kidney structure. Such anomalies consist of underdevelopment of the renal parenchyma or the formation of cysts in the renal tissue.
Duplication of the kidneys and pyelocaliceal system. Signs of kidney duplication on ultrasound
Kidney doubling is the most common anomaly kidney It occurs in women 2 times more often than in men. Kidney doubling explained congenital anomaly germ layers of the ureters. Doubled buds are conventionally divided into top part and lower, of which the upper bud is usually less developed. Doubling differs from an additional bud in that both parts are tied friend with each other and are covered with one fibrous capsule. The accessory kidney is less common, but has its own blood supply and capsule. Kidney duplication can be complete or incomplete.Kidney duplication can be of two types:
- Full doubling. With this type of duplication, both parts have their own pyelocaliceal system, artery and ureter.
- Incomplete doubling. It is characterized by the fact that the ureters of both parts unite before emptying into the bladder. Depending on the degree of development of the upper part, it may have its own artery and pyelocaliceal system.
Underdevelopment ( hypoplasia, dysplasia) kidneys on ultrasound
Underdevelopment of the kidneys can occur in two ways. One of them is hypoplasia - a condition in which the kidney is reduced in size, but functions as well as normal kidney. Another option is dysplasia. This term refers to a condition in which the kidney is not only reduced in size, but also structurally defective. With dysplasia, the parenchyma and CL of the kidneys are significantly deformed. In both cases, the kidney on the opposite side is enlarged to compensate functional impairment underdeveloped kidney.With renal hypoplasia, ultrasound reveals a smaller organ. Its length on ultrasound is less than 10 centimeters. Ultrasound can also determine the function of an underdeveloped kidney. In a functioning kidney, the arteries have a normal width ( 5 mm at the gate), and the pyelocaliceal system is not dilated. However, with dysplasia the opposite picture is observed.
Signs of kidney dysplasia on ultrasound are:
- expansion of the maxillofacial area of more than 25 mm in the area of the pelvis;
- reduction in parenchyma thickness;
- narrowing of the renal arteries;
- narrowing of the ureters.
Kidney prolapse ( nephroptosis) on ultrasound. Wandering buds
Nephroptosis is a condition in which the kidney moves down from its bed when the body position changes. Normally, the movement of the kidneys during their transition from vertical to horizontal position does not exceed 2 cm. However, due to various factors (injuries, excessive physical activity, muscle weakness ) the kidney may acquire pathological mobility. Nephroptosis occurs in 1% of men and about 10% of women. In cases where the kidney can be moved by hand, it is called a wandering kidney.Nephroptosis has three degrees:
- First degree. When inhaling, the kidney partially moves down from the hypochondrium and is palpated, and returns back during exhalation.
- Second degree. IN vertical position the kidney completely emerges from the hypochondrium.
- Third degree. The kidney descends below the iliac crest into the pelvis.
Ultrasound reveals nephroptosis in most cases. The kidney may not be detected on a routine scan in the upper lateral abdomen. If renal prolapse is suspected, an ultrasound scan is performed in three positions - lying, standing and on the side. The diagnosis of nephroptosis is made in the case of an abnormally low position of the kidneys, their great mobility when changing body position or when breathing. Ultrasound also helps identify complications caused by changes in the position of the kidneys.
Kidney cyst on ultrasound
A cyst is a cavity in the kidney tissue. It has an epithelial wall and a fibrous base. Kidney cysts can be congenital or acquired. Congenital cysts develop from cells of the urinary tract that have lost connection with the ureters. Acquired cysts form at the site of pyelonephritis, kidney tuberculosis, tumors, heart attack, as a residual formation.A kidney cyst usually does not appear clinical symptoms and is detected incidentally during ultrasound examination. When the kidney size is up to 20 mm, the cyst does not cause compression of the parenchyma and functional impairment. A cyst larger than 30 mm is an indication for puncture.
On a kidney ultrasound, the cyst appears as a round, black, anechoic formation. The cyst is surrounded by a hyperechoic rim fibrous tissue. The cyst may contain dense areas that are blood clots or fossils. The cyst may have septa, which are also visible on ultrasound. Multiple cysts are not so common; they need to be differentiated from polycystic kidney disease, a disease in which the kidney parenchyma is almost completely replaced by cysts.
When performing an ultrasound with a water or diuretic load, the size of the cyst does not change, in contrast to the pyelocaliceal system, which expands during this study. On color Doppler imaging, the cyst does not produce color signals because there is no blood supply to its wall. If vessels are found around the cyst, this indicates its degeneration into a tumor.
Puncture of cysts using ultrasound guidance
Ultrasound examination is indispensable for the treatment of kidney cysts. Using ultrasound, the size and position of the cyst and its accessibility for puncture are assessed. Under control ultrasound image A special needle is inserted through the skin and fixed to the puncture sensor. The location of the needle is checked by the image on the screen.After the wall of the cyst is punctured, its contents are removed and examined in the laboratory. The cyst may contain serous fluid, urine, blood, or pus. Then a special liquid is injected into the cyst cavity. It destroys the epithelium of the cyst and resolves over time, causing the cyst cavity to be replaced with connective tissue. This method of treating cysts is called sclerotherapy.
For the treatment of cysts up to 6 cm in diameter, cyst sclerotherapy is effective. In certain positions of cysts or their large sizes Only surgical removal of the cysts is possible.
Polycystic kidney disease on ultrasound
Polycystic disease is a congenital kidney disease. Depending on the type of inheritance, it can manifest itself in childhood or in adults. Polycystic disease is genetic disease, so he is not cured. The only treatment for polycystic disease is kidney transplantation.For polycystic disease genetic mutation leads to disruption of the fusion of nephron tubules with the primary collecting ducts. Because of this, multiple cysts form in the cortex. Unlike simple cysts, with polycystic disease the entire cortex is gradually replaced by cysts, causing the kidney to become nonfunctional. In polycystic disease, both kidneys are affected equally.
On ultrasound, the polycystic kidney is enlarged in size and has a lumpy surface. In the parenchyma, multiple anechoic formations are found that do not connect with pyelocalyceal system. The cavities on average range in size from 10 to 30 mm. In newborns with polycystic kidney disease, a narrowing of the chest and an empty bladder are characteristic.
Medullary spongy kidney on kidney ultrasound
This disease is also a congenital pathology, however, unlike polycystic disease, cysts are formed not in the cortex, but in the medulla. Due to deformation of the collecting ducts of the pyramids, the kidney becomes like a sponge. The cyst cavities in this pathology range in size from 1 to 5 mm, that is, much smaller than in polycystic disease.The medullary spongy kidney functions normally for a long time. Unfortunately, this disease is a provoking factor for urolithiasis and infections ( pyelonephritis). In this case, unpleasant symptoms may appear in the form of pain and urination problems.
On ultrasound, a medullary spongy kidney is usually not detected, since there are no ultrasound machines with a resolution greater than 2–3 mm. With medullary spongy kidney, the cysts are usually smaller. A decrease in the echogenicity of the renal medulla may be suspected.
Excretory urography is used to diagnose this disease. This method applies to X-ray diagnostics. With excretory urography, the filling of the urinary tract is observed. X-ray contrast agent. The medullary kidney is characterized by the formation of a “bouquet of flowers” in the medulla on excretory urography.
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